Save
Email
Print
ShareFeb. 24, 2009 — Alcohol and iron are believed to have a synergistic effect in the development of liver injury. Furthermore, alcohol enhances iron absorption. Primary hemochromatosis is a genetic disorder, mostly resulting from mutations in the HFE gene, with a disturbance in the iron metabolism which leads to iron accumulation that may eventually result in liver disease. However, data regarding an association between iron metabolism, HFE mutations and alcoholic liver disease are inconclusive at present.
A research team led by Professor Helena Cortez-Pinto, from Hospital Santa Maria in Lisbon, studied a group of heavy drinkers with and without liver disease. A high prevalence of iron overload was found in alcoholics, which appeared to be related to the development of liver disease [odds ration for having liver disease in alcoholics with transferrin saturation greater than 45% was 2.2 (95% CI 1.37-3.54)]. Regarding HFE mutations, only H63D was found to be associated with alcoholic liver disease [odds ratio 1.57 (95% CI 1.02-2.40)]. Alcoholics who were heterozygotes for H63D mutation and had evidence of iron overload, showed an even greater risk of developing liver disease [odds ratio 2.17 (95% CI 1.42-3.32)].
Based on these findings, it appears that iron overload is an important co-factor in the development of liver disease in alcoholics. Even heterozygotes for H63D mutation, who classically do not develop liver disease, had an increased susceptibility to liver disease, in the presence of excessive alcohol consumption.
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by World Journal of Gastroenterology, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Machado MV, Ravasco P, Martins A, Almeida MR, Camilo ME, Cortez-Pinto H. Iron homeostasis and H63D mutations in alcoholics with and without liver disease. World J Gastroenterol, 2009; 15(1): 106-111 [link]
Note: If no author is given, the source is cited instead.
more 
